The nodular form of interstitial myocarditis is usually purulent, the pathology of which has just been described.
Eppinger has termed toxic myolysis of the heart in diphtheria an redematous infiltration of the inyocardium, breaking the course of the muscle fibres, with vacuolization and complete dissolution. He believes that the diagnosis of cardiac death from diphtheria can be made with certainty from these changes in the heart.
• As regards the pathogenesis of the various forms of myocarditis, different microorganisms which produce inflammation have been found in the wall of the heart itself, in a series of cases of the interstitial forms (pus cocci, typhoid bacilli, bacillus pyocyaneus). Doubtless, how ever, the toxins of the infectious diseases play the principal part, in diphtheria, scarlet fever and typhoid fever especially-, the last only rarely exerting in childhood that serious influence upon the heart which it has upon adults.
Winogradow found important pathologic anatomic changes in the automatic ganglia of the heart in 22 cases of congenital syphilis of infants. With interstitial growth of the connective tissue and changes in the blood vessels, severe degenerations of the ganglion cells have frequently been found. B. Fischer described serious syphilitic changes in the myocardium with aneurysmic dilatation of the conus venosus, in St boy of five years.
Symptoms and symptoms of acute parenchymatous myocarditis comist of diminution in the power of the heart, which is recognized by marked weakness of the pulse, impossibility of feeling the apex-beat and low heart sounds nit]) embryocardial rylithm. The pulse is as a rule enormously accelerated and the second sound of the heart is frequently inaudible. These children show high-grade dyspncea, a deep pallor, cold cyanotic extremities and peripheral parts of the body, in contrast to the rest of the body surface, which usually feels very hot, because the disease produces fever. These children are tormented by a peculiar vexing restlessness which cannot be bettered and show rapid respiration, especially high in the chest, combined with movements of the alm nasi mith respiration.
In rare cases of chronic parenchymatous myocarditis after infectious diseases, belonging to later childhood, there is retardation of the pulse, with arrhythmia and irregular respiration, at times abnormally slow, and then again very rapid. The rapid rise in the pulse-rate and respira tion, nith the slightest bodily or mental excitement is characteristic of this form of myocarditis in children.
The symptomatology of parenchymatous myocarditis is on the whole not very well outlined, so that the disease in many cases remains unrecognized during life (Zuppinger).
Still more uncertain is the symptom-complex of acute interstitial myocarditis. Symptoms of cardiac weakness and dilatation am com bined with the setious symptoms of the fundamental disease. When, in the course of an acute infectious disease, severe symptoms of dysp ncea, weak rapid pulee and cyanosis develop gradually, unexplained by any intercurrent pulmonary disease, the diagnosis of the presence of myocarditis is justified, though the question whether it be an inter stitial or parenchymatous myocarditis remains undecided.
As in all morbid processes which lead to relaxation of the heart muscle, dilatation of the cardiac cavities (sonietimes high-grade, Cro chet) with relative inability of the valvular apparatus to close, thus producing murmurs. may also occur in myocarditis. The diagnosis of the myocarditic processes which follow acute and chronic endopericar ditis, symphysis pericardii and congenital heart lesions cannot be made. Loss of compensation and death from chronic affections of the heart in childhood are often the result of myoearditic processes which have appeared doling new attacks of rheumatism or in the course of inter current infectious diseases.
Intracardial thrombosis, with emboli, has repeatedly been observed in the various forms of myocarditis, especially diphtheritic myocarditis (Degny and Weill, Leyden).